Decentralized Greedy-Based Algorithm for Smart Energy Management in Plug-in Electric Vehicle Energy Distribution Systems

Variations in electricity tariffs arising due to stochastic demand loads on the power grids have stimulated research in finding optimal charging/discharging scheduling solutions for electric vehicles (EVs). Most of the current EV scheduling solutions are either centralized, which suffer from low reliability and high complexity, while existing decentralized solutions do not facilitate the efficient scheduling of on-move EVs in large-scale networks considering a smart energy distribution system. Motivated by smart cities applications, we consider in this paper the optimal scheduling of EVs in a geographically large-scale smart energy distribution system where EVs have the flexibility of charging/discharging at spatially-deployed smart charging stations (CSs) operated by individual aggregators. In such a scenario, we define the social welfare maximization problem as the total profit of both supply and demand sides in the form of a mixed integer non-linear programming (MINLP) model. Due to the intractability, we then propose an online decentralized algorithm with low complexity which utilizes effective heuristics to forward each EV to the most profitable CS in a smart manner. Results of simulations on the IEEE 37 bus distribution network verify that the proposed algorithm improves the social welfare by about 30% on average with respect to an alternative scheduling strategy under the equal participation of EVs in charging and discharging operations. Considering the best-case performance where only EV profit maximization is concerned, our solution also achieves upto 20% improvement in flatting the final electricity load. Furthermore, the results reveal the existence of an optimal number of CSs and an optimal vehicle-to-grid penetration threshold for which the overall profit can be maximized. Our findings serve as guidelines for V2G system designers in smart city scenarios to plan a cost-effective strategy for large-scale EVs distributed energy management

Calcific aortic valve disease and hypertension

This review addresses the role of hypertension in precipitating Calcific aortic valve disease (CAVD) and the therapeutic potential of anti-hypertensive interventions to ameliorate CAVD. CAVD was originally considered to be a degenerative disease representing the "wear and tear" of the aortic valves. More recently both conceptually and experimentally, CAVD has come to be considered the result of an active disease process, Whilst, there are some common factors in the pathology and risk factors for atherosclerosis and CAVD there are also some distinct differences. Hypertension is an established risk factor for coronary artery disease and has been recognised as a risk factor for CAVD. Angiotensin converting enzyme inhibitors have been found to have beneficial effects in CAVD and as in atherosclerosis such effects may be due to the blood pressure lowering action but also to direct pleiotropic effects on the biochemical and cellular mechanisms of disease progression in the respective tissues. The very high prevalence of hypertension in the community coupled with an aging population, a risk factor associated with both hypertension and CAVD, infers that hypertension will be one of the predominant factors that increase the impact of CAVD on human health in the coming decades

Mesalamine-Induced Myocarditis and Coronary Vasculitis in a Pediatric Ulcerative Colitis Patient: A Case Report

Mesalamine-containing products are often a first-line treatment for ulcerative colitis. Severe adverse reactions to these products, including cardiovascular toxicity, are rarely seen in pediatric patients. We present a case of a 16-year-old boy with ulcerative colitis treated with Asacol, a mesalamine-containing product, who developed sudden onset chest pain after four weeks on therapy. Serial electrocardiograms showed nonspecific ST segment changes, an echocardiogram showed mildly decreased left ventricular systolic function with mild to moderate left ventricular dilation and coronary ectasia, and his troponins were elevated. Following Asacol discontinuation, his chest pain resolved, troponins were trending towards normal, left ventricular systolic function normalized, and coronary ectasia improved within 24 hours suggesting an Asacol-associated severe drug reaction. Mesalamine-induced cardiovascular toxicity, although rare, may represent a life-threatening disorder. Therefore, every patient presenting with acute chest pain should receive a workup to rule out this rare drug-induced disorder

p38 MAP kinase mediated proteoglycan synthesis as a target for the prevention of atherosclerosis

The major underlying pathology of most cardiovascular disease is the chronic inflammatory disease of atherosclerosis. Type 2 diabetes, also recognised as an inflammatory condition, accelerates the development of atherosclerosis. Current therapies for atherosclerosis target risk factors such as elevated blood lipids and hypertension and are of strong but limited efficacy. The "response to retention" hypothesis states that atherosclerosis is initiated by the accumulation of lipids through binding to extracellular matrix, and this is specifically the glycosaminoglycan (GAG) chains on proteoglycans. Many vasoactive agonists stimulate changes in the structure of the GAGs which increase lipid binding and the relevant signalling pathways are a potential therapeutic target. It has recently been demonstrated that the actions of transforming growth factor b; on vascular smooth muscle proteoglycan synthesis involves signalling through p38 MAP kinase and inhibition of this pathway reduces binding of lipids. Inhibition of p38 MAP kinase will elicit a wide spread antiinflammatory response which may alleviate some of the deleterious processes in cardiovascular tissues. This article explores the potential for the actions of p38 MAP kinase inhibitors directed at proteoglycan synthesis in vascular smooth muscle to contribute to the beneficial outcomes from targeting p38 MAP kinase for the prevention of cardiovascular disease

Reliability and Reproducibility of Landmark Identification in Unilateral Cleft Lip and Palate Patients: Digital Lateral Vis-A-Vis CBCT-Derived 3D Cephalograms

Background: The aim of the retrospective observational study was to compare the precision of landmark identification and its reproducibility using cone beam computed tomography-derived 3D cephalograms and digital lateral cephalograms in unilateral cleft lip and palate patients. Methods: Cephalograms of thirty-one (31) North Indian children (18 boys and 13 girls) with a unilateral cleft lip and palate, who were recommended for orthodontic treatment, were selected. After a thorough analysis of peer-reviewed articles, 20 difficult-to-trace landmarks were selected, and their reliability and reproducibility were studied. These were subjected to landmark identification to evaluate interobserver variability; the coordinates for each point were traced separately by three different orthodontists (OBA, OBB, OBC). Statistical analysis was performed using descriptive and inferential statistics with paired t-tests to compare the differences measured by the two methods. Real-scale data are presented in mean ± SD. A p-value less than 0.05 was considered as significant at a 95% confidence level. Results: When comparing, the plotting of points posterior nasal spine (PNS) (p < 0.05), anterior nasal spine (ANS) (p < 0.01), upper 1 root tip (p < 0.05), lower 1 root tip (p < 0.05), malare (p < 0.05), pyriforme (p < 0.05), porion (p < 0.01), and basion (p < 0.05) was statistically significant. Conclusion: In patients with a cleft lip and palate, the interobserver identification of cephalometric landmarks was significantly more precise and reproducible with cone beam computed tomography -derived cephalograms vis-a-vis digital lateral cephalograms

Comparative Evaluation of Azadirachta indica (Neem) Chip and Soft Tissue Diode Lasers as a Supplement to Phase i Periodontal Therapy in Localized Chronic Moderate Periodontitis: A Randomized Controlled Clinical Trial

Introduction. The current trial aimed to assess and compare the efficacy of neem chip and diode laser as a local drug delivery (LDD) agent as a supplement to phase I periodontal therapy in treatment of localized chronic moderate periodontitis. Materials and Methodology. Fourteen systemically healthy participants with 4-6 mm deep periodontal pockets at least in three quadrants (with no alveolar bony defect amenable to respective or regenerative osseous surgery, as seen in orthopantomograph) were selected for the trial. One week after phase I therapy, 10% absorbable chip of neem (commercially prepared by staff of a pharmacy college, Sheriguda, India) was placed in the periodontal pocket on one site, and soft tissue diode laser pocket sterilization was performed on the other site of the arch. Remaining one site was considered as a control. Parameters recorded clinically were plaque index (PI), papillary bleeding index (PBI), probing pocket depth (PPD), and relative attachment level (RAL) measured at baseline, 21st day, and one month postoperatively. Results. Statistically significant improvements were observed in all clinical parameters at one month as compared to baseline for both treatment groups. Conclusion. Neem chip supplemented with phase I therapy showed best improvement in clinical parameters followed by laser supplemented with phase I therapy in comparison to phase I therapy alone at one month follow-up. Clinical Significance. Neem chips are nature's products, affordable without side effects, with a potential to be used as a local drug delivery agent in treating moderate chronic periodontitis

Biophysical studies of the gingival epithelium

Objectives: As the gingival epithelial cells undergo transition between the surface, crevicular and junctional areas, it is reported that their resting potential could also get altered due to change/variations in the membrane transport protein composition. Hence, the purpose of the present study is (i) to study the biophysical properties of the surface, the crevicular, and the junctional epithelial gingival cells and to assess their implications to the cell to cell and the cell to tooth attachment mechanisms; (ii) to study the effect of certain delipidifying agents such as Sodium Deoxycholate (DOC) and Sodium Dodecyl Sulfate (SDS) on the transmembrane electrical activity of the gingival epithelial cells; and, (iii) to study the histological changes due to these treatments and assess their bearings on the biophysical observations. Materials and Methods: The biophysical and histological investigations on the healthy human gingival epithelium were carried out on the fresh biopsy material obtained from a homogeneous group of willing donors between 11-15 years of age, who were advised for extraction of first premolar due to orthodontic reasons. The biophysical measurement involved recording of the transmembrane potentials using glass ultra-microelectrodes. For histologic studies, the hematoxylin and eosin (H&E) staining of the tissue sections was performed. Results: The mean values of the membrane potential in the three types of the gingival epithelium cells vary appreciably. While it was lowest in the junctional cells (2.83 ± 0.98 mV), it was highest in the surface epithelial cells (22.96 ± 5.19 mV). The crevicular cells showed a value greater than the junctional cells but lesser than the surface cells (9.3 ± 1.73 mV). Conclusion: The membrane transport protein density appears to decrease in the following order: surface > crevicular > junctional cells. The crosslinking force of calcium (Ca 2+ ) ions with their increased magnitude from the junctional epithelial cells to the cementum or enamel of the tooth appears to be the most convincing model of the epithelial attachment at the Dentoenamel (DE) junction

Mesalamine-Induced Myocarditis and Coronary Vasculitis in a Pediatric Ulcerative Colitis Patient: A Case Report

Mesalamine-containing products are often a first-line treatment for ulcerative colitis. Severe adverse reactions to these products, including cardiovascular toxicity, are rarely seen in pediatric patients. We present a case of a 16-year-old boy with ulcerative colitis treated with Asacol, a mesalamine-containing product, who developed sudden onset chest pain after four weeks on therapy. Serial electrocardiograms showed nonspecific ST segment changes, an echocardiogram showed mildly decreased left ventricular systolic function with mild to moderate left ventricular dilation and coronary ectasia, and his troponins were elevated. Following Asacol discontinuation, his chest pain resolved, troponins were trending towards normal, left ventricular systolic function normalized, and coronary ectasia improved within 24 hours suggesting an Asacol-associated severe drug reaction. Mesalamine-induced cardiovascular toxicity, although rare, may represent a life-threatening disorder. Therefore, every patient presenting with acute chest pain should receive a workup to rule out this rare drug-induced disorder

Smad 2 and p38 MAP mediated signalling of proteoglycan synthesis in vascular smooth muscle

Atherosclerosis is the underlying pathological process of most cardiovascular disease. A critical component of the "response to retention" hypothesis of atherogenesis is proteoglycan/ low density lipoprotein (LDL) binding. Transforming growth factor (TGF- ) is present in atherosclerotic lesions, regulates vascular smooth muscle cell (VSMC) proteoglycan synthesis via an unknown signaling pathway, and increases proteoglycan/ LDL binding. This pathway was investigated using the activin receptor-like kinase 5 (ALK5) inhibitor SB431542 and inhibitors of p38 MAP kinase as a possible downstream or alternative mediator. TGF- stimulated and SB431542 inhibited the phosphorylation of Smad2/3. In human VSMC, TGF- increased [35S]sulfate incorporation into proteoglycans associated with a 19% increase in glycosaminoglycan (GAG) chain size by size exclusion chromatography. SB431542 caused a concentration-dependent decrease in TGF- -mediated [35S]sulfate incorporation with 92% inhibition at 3 M. Two different p38MAPkinase inhibitors, SB203580 and SB202190, but not the inactive analogue SB202474, concentrationdependently blocked TGF- -mediated [35S]sulfate incorporation. TGF- increased [3H]glucosamine incorporation into glycosaminoglycans by 180% and [35S]Met/Cys incorporation into proteoglycan core proteins by 35% with both effects completely inhibited by SB431542. Blocking both Smad2/3 and p38 MAP kinase pathways prevented the effect of TGF- to increase proteoglycan to LDL binding. TGF- mediates its effects on proteoglycan synthesis in VSMCs via the ALK5/Smad2/3 phosphorylation pathway as well as via the p38 MAP kinase signaling cascade. Further studies of downstream pathways controlling proteoglycan synthesis may identify potential therapeutic targets for the prevention of atherosclerosis and cardiovascular disease